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. 2016 Jun 15;7(29):46127–46141. doi: 10.18632/oncotarget.10060

Figure 6. In vitro and in vivo drug sensitivity analyses of GC cells with ARID1A-depletion.

Figure 6

A. SGC-7901 with endogenous ARID1A-depletion was sensitized to LY294002 comparing with the control. The p value was calculated using F-test and p < 0.05 was considered as statistically significant. B. Increased sensitivity of HGC-27 with ARID1A-silencing to LY294002. C and D. Increased sensitivity of SGC-7901 and HGC-27 with ARID1A-silencing to AT7867, an inhibitor against AKT and p70S6K. E. Xenograft mouse model analysis of SGC-7901 with deficient ARID1A. The SGC-7901 cells with ARID1A knockdown or control gene silencing (Sh-Luciferase) were injected subcutaneously into both flanks of nude mice. After the tumors were established, the mice were treated with LY294002 or PBS as a control by intraperitoneal injection. The mice bearing tumors were shown to the right. Sh-Luc, Sh-Luciferase. Sh-AR, Sh-ARID1A. F. The xenograft tumors were measured every two days and the volumes were calculated. The arrow indicates the time point the mice received LY294002 treatment. The p values above the curve indicate the significant divergence of the volumes between LY294002 and PBS treated tumors of sh2-ARID1A cells.